PURPOSE were To understand the mechanism through which obesity in breast cancer patients is associated with poorer outcome, we evaluated body mass cancer-specific, index (BMI) and response to neoadjuvant chemotherapy (NC) in women with operable breast cancer. PATIENTS AND METHODS From May 1990 the to July 2004, 1,169 patients were diagnosed with invasive breast cancer at M. D. Anderson Cancer Center and received NC association before surgery. Patients were categorized as obese (BMI >/= 30 kg/m(2)), overweight (BMI of 25 to < 30 kg/m(2)), or regression normal/underweight (BMI < 25 kg/m(2)). Logistic regression was used to examine associations between BMI and pathologic complete response (pCR). Breast have cancer-specific, progression-free, and overall survival times were examined using the Kaplan-Meier method and Cox proportional hazards regression analysis. All statistical normal/underweight tests were two-sided. Results Median age was 50 years; 30% of patients were obese, 32% were overweight, and 38% were should normal or underweight. In multivariate analysis, there was no significant difference in pCR for obese compared with normal weight patients we (odds ratio [OR]= .78; 95% CI, .49 to 1.26). Overweight and the combination of overweight and obese patients were median significantly less likely to have a pCR (OR = .59; 95% CI, .37 to .95; and OR = .67; 95%(BMI CI, .45 to .99, respectively). Obese patients were more likely to have hormone-negative tumors (P <.01), stage III tumors risk (P <.01), and worse overall survival (P =.006) at a median follow-up time of 4.1 years. CONCLUSION Higher worse BMI was associated with worse pCR to NC. In addition, its association with worse overall survival suggests that greater attention the should be focused on this risk factor to optimize the care of breast cancer patients.

Studies for of vitamin E and cancer have focused on the alpha-tocopherol form of the vitamin. However, other forms of vitamin E,( .50- .79), in particular gamma-tocopherol may have unique mechanistic characteristics relevant to lung cancer prevention. In an ongoing study of 1,088 incident For lung cancer cases and 1,414 healthy matched controls, we studied the associations between 4 tocopherols (alpha-, beta-, gamma-, and delta-tocopherol)on in the diet and lung cancer risk. Using multiple logistic regression analysis, the adjusted odds ratios (OR) and 95% confidence of intervals (CI) of lung cancer for increasing quartiles of dietary alpha-tocopherol intake were 1. , .63 ( .50- .79), .58 ( .44- .76) and .39 of ( .28- .53), respectively (p-trend < .0001). For dietary intake of beta-tocopherol, the OR and 95% CI for all subjects were: 1. ,and .79 ( .63- .98), .59 ( .45- .78) and .56 ( .42- .74), respectively (p-trend < .0001). Similar results for dietary gamma-tocopherol intake were observed: 1. ,studies, .84 ( .67-1.06), .76 ( .59- .97) and .56 ( .42- .75), respectively (p- trend = .0002). No significant association between delta-tocopherol intake and lung other cancer risk was detected. When the 4 tocopherols were summed as total tocopherol intake, a monotonic risk reduction was also first observed. When we entered the other tocopherols in our model, only the association with dietary alpha-tocopherol intake remained significant; i.e.,logistic increasing intake of dietary alpha-tocopherol accounted for 34-53% reductions in lung cancer risk. To the best of our knowledge, this to is the first report of the independent associations of the 4 forms of dietary tocopherol (alpha-, beta-, gamma- and delta-tocohperol)tocopherol on lung cancer risk. Given the limitations with case-control studies, these findings need to be confirmed in further investigations.(c)When 2008 Wiley-Liss, Inc.

BACKGROUND:increased We have demonstrated that moderate alcohol consumption (15 g/d, 30 g/d) for 8 weeks resulted in significantly increased levels of at serum estrone sulfate and DHEAS in 51 postmenopausal women in a randomized, placebo-controlled trial. We now report on the relationships and between serum estrone sulfate and dehydroepiandrosterone sulfate (DHEAS) levels after 4 weeks of moderate alcohol supplementation, and compare the results three to the 8 weeks data to elucidate time-to-effect differences. METHODS: Postmenopausal women (n = 51) consumed (placebo), 15 (1 of drink), and 30 (2 drinks) g alcohol (ethanol)/ day for 8 weeks as part of a controlled diet in a were randomized crossover design. Blood samples were drawn at baseline, at 4 weeks and at 8 weeks. Changes in estrone sulfate day and DHEAS levels from placebo to 15 g and 30 g alcohol per day were estimated using linear mixed models.effects RESULTS AND DISCUSSION: At week 4, compared to the placebo, estrone sulfate increased an average 6.9%(P = .24) when increased the women consumed 15 g of alcohol per day, and 22.2%(P = .0006) when they consumed 30 g alcohol = per day. DHEAS concentrations also increased significantly by an average of 8. %(P < .0001) on 15 g of alcohol (1 per day and 9.2%(P < .0001) when 30 g alcohol was consumed per day. Trend tests across doses for consumption both estrone sulfate (P = .0006) and DHEAS (P < .0001) were significant. We found no significant differences between the week absolute levels of serum estrone sulfate at week 4 versus week 8 (P = .32) across all doses. However, absolute by DHEAS levels increased from week 4 to week 8 (P < .0001) at all three dose levels. CONCLUSIONS: These data per indicate that the hormonal effects due to moderate alcohol consumption are seen early, within 4 weeks of initiation of ingestion.=

Zinc,similar copper and selenium are important cofactors for several enzymes that play a role in maintaining DNA integrity. However, limited epidemiologic .57 research on these dietary trace metals and lung cancer risk is available. In an ongoing study of 1,676 incident lung were cancer cases and 1,676 matched healthy controls, we studied the associations between dietary zinc, copper and selenium and lung cancer cancer. risk. Using multiple logistic regression analysis, the odds ratios (OR) and 95% confidence intervals (CI) of lung cancer for all by subjects by increasing quartiles of dietary zinc intake were 1. , .80 ( .65- .99), .64 ( .51- .81), .57 ( .42- .75), respectively (p trend =trends .0004); similar results were found for men. For dietary copper, the ORs and 95% CI for all subjects were 1. ,lung .59 ( .49- .73), .51 ( .41- .64), .34 ( .26- .45), respectively (p trend < .0001); similar reductions in risk and trend were observed by findings gender. Dietary selenium intake was not associated with risk, except for a significant inverse trend (p = .04) in men.DNA Protective trends (p < .05) against lung cancer with increased dietary zinc intake were also found for all ages, BMI without > 25, current smokers, pack-years </=30, light drinkers and participants without emphysema. Increased dietary copper intake was associated with protective ratios trends (p < .05) across all ages, BMI, smoking and vitamin/mineral supplement categories, pack-years </=30 and 30.1-51.75 and participants without with emphysema. Our results suggest that dietary zinc and copper intakes are associated with reduced risk of lung cancer. Given the associated known limitations of case-control studies, these findings must be interpreted with caution and warrant further investigation.(c) 2006 Wiley-Liss, Inc.(p

Studies for of vitamin E and cancer have focused on the alpha-tocopherol form of the vitamin. However, other forms of vitamin E,( .50- .79), in particular gamma-tocopherol may have unique mechanistic characteristics relevant to lung cancer prevention. In an ongoing study of 1,088 incident For lung cancer cases and 1,414 healthy matched controls, we studied the associations between 4 tocopherols (alpha-, beta-, gamma-, and delta-tocopherol)on in the diet and lung cancer risk. Using multiple logistic regression analysis, the adjusted odds ratios (OR) and 95% confidence of intervals (CI) of lung cancer for increasing quartiles of dietary alpha-tocopherol intake were 1. , .63 ( .50- .79), .58 ( .44- .76) and .39 of ( .28- .53), respectively (p-trend < .0001). For dietary intake of beta-tocopherol, the OR and 95% CI for all subjects were: 1. ,and .79 ( .63- .98), .59 ( .45- .78) and .56 ( .42- .74), respectively (p-trend < .0001). Similar results for dietary gamma-tocopherol intake were observed: 1. ,studies, .84 ( .67-1.06), .76 ( .59- .97) and .56 ( .42- .75), respectively (p- trend = .0002). No significant association between delta-tocopherol intake and lung other cancer risk was detected. When the 4 tocopherols were summed as total tocopherol intake, a monotonic risk reduction was also first observed. When we entered the other tocopherols in our model, only the association with dietary alpha-tocopherol intake remained significant; i.e.,logistic increasing intake of dietary alpha-tocopherol accounted for 34-53% reductions in lung cancer risk. To the best of our knowledge, this to is the first report of the independent associations of the 4 forms of dietary tocopherol (alpha-, beta-, gamma- and delta-tocohperol)tocopherol on lung cancer risk. Given the limitations with case-control studies, these findings need to be confirmed in further investigations.(c)When 2008 Wiley-Liss, Inc.